<i>H. pylori</i> -CSAs and CagA seropositivity and the risk of stomach adenocarcinoma overall, cardia site and non-cardia site.

<p>* Odds ratios (ORs) were derived from conditional logistic regression models.</p

Flowchart for identifying stomach adenocarcinoma cases.

<p>In total 105 stomach cancers (ICD-7 code 151) which occurred at least 5 years after blood sample collection were identified during follow-up. Among these, 27 were excluded due to either missing serum samples or the fact that the cancers were found incidentally at autopsy. For the remaining 78 cases, medical records related to cancer diagnosis for 68 cases were successfully retrieved. After review, 9 cases were deemed to be tumors other than stomach adenocarcinoma. Among the remaining 59 stomach adenocarcinoma cases, 15 stomach adenocarcinoma cases were determined to be cardia adenocarcinoma and 41 as non-cardia stomach adenocarcinoma. In 3 stomach adenocarcinoma cases it was not possible to determine the exact origin in the stomach.</p

Characteristics of the stomach adenocarcinoma cases and their matched controls.

<p>* Defined as serum pepsinogen I<25 ug/l or pepsinogen I:II ratio <3 at time of initial serum collection.</p

A Meta-Analysis of Oxidative Stress Markers in Depression

<div><p>Object</p><p>Studies have suggested that depression was accompanied by oxidative stress dysregulation, including abnormal total antioxidant capacity (TAC), antioxidants, free radicals, oxidative damage and autoimmune response products. This meta-analysis aims to analyse the clinical data quantitatively by comparing the oxidative stress markers between depressed patients and healthy controls.</p><p>Methods</p><p>A search was conducted to collect the studies that measured the oxidative stress markers in depressed patients. Studies were searched in Embase, Medline, PsychINFO, Science direct, CBMDisc, CNKI and VIP from 1990 to May 2015. Data were subjected to meta-analysis by using a random effects model for examining the effect sizes of the results. Bias assessments, heterogeneity assessments and sensitivity analyses were also conducted.</p><p>Results</p><p>115 articles met the inclusion criteria. Lower TAC was noted in acute episodes (AEs) of depressed patients (<i>p</i><0.05). Antioxidants, including serum paraoxonase, uric acid, albumin, high-density lipoprotein cholesterol and zinc levels were lower than controls (<i>p</i><0.05); the serum uric acid, albumin and vitamin C levels were increased after antidepressant therapy (<i>p</i><0.05). Oxidative damage products, including red blood cell (RBC) malondialdehyde (MDA), serum MDA and 8-F₂-isoprostanes levels were higher than controls (<i>p</i><0.05). After antidepressant medication, RBC and serum MDA levels were decreased (<i>p</i><0.05). Moreover, serum peroxide in free radicals levels were higher than controls (<i>p</i><0.05). There were no differences between the depressed patients and controls for other oxidative stress markers.</p><p>Conclusion</p><p>This meta-analysis supports the facts that the serum TAC, paraoxonase and antioxidant levels are lower, and the serum free radical and oxidative damage product levels are higher than controls in depressed patients. Meanwhile, the antioxidant levels are increased and the oxidative damage product levels are decreased after antidepressant medication. The pathophysiological relationships between oxidative stress and depression, and the potential benefits of antioxidant supplementation deserve further research.</p></div

The comparisons of effect sizes for serum TAC (A), serum non-enzymatic antioxidants (B), red blood cell enzymatic antioxidants (C), serum enzymatic antioxidants (D), serum free radicals (E) and serum oxidative damage products (F) in acute episodes between depressed patients and controls (red bar) and in comparison before and after treatment of depressed patients (yellow bar).

<p>Positive effect sizes (bars go upwards) indicate that the marker levels in depressed patients were higher than controls or increased after antidepressant therapy; negative effect sizes (bars go downwards) indicate that marker levels were lower than controls or decreased after antidepressant therapy. *<i>p</i> < 0.05, **<i>p</i> < 0.01, ***<i>p</i> < 0.001. TAC, total antioxidant capacity; HDL-C, high-density lipoprotein cholesterol; SOD, superoxide dismutase; GPX, glutathione peroxidase; CAT, catalase; GR, glutathione reductase; PON, paraoxonase; MDA, malondialdehyde; 8-<i>iso</i>-PGF_2α, 8-F2-isoprostanes; PCC, oxidation protein product.</p

Averaged neuromagnetic responses (overlay of all 148 channels) to the auditory stimuli in the control subject.

<p>Averaged neuromagnetic responses (overlay of all 148 channels) to the auditory stimuli in the control subject.</p

Locations of M100 dipole sources in an individual control subject, an individual schizophrenia, and an individual bipolar disorder on axial T1- weighted images.

<p>Locations of M100 dipole sources in an individual control subject, an individual schizophrenia, and an individual bipolar disorder on axial T1- weighted images.</p